Epidemiologic studies suggest that chronic social stressors are related to increased incidence of infectious upper respiratory disease. However, these studies are correlational and causal inference is limited. Moreover, this work does not address how stressors influence disease susceptibility nor does it account for the vast individual differences in stressor influences on immunity and disease. Employing a nonhuman primate model, the proposed work: a) provides an experimental test of the effects of a chronic social stressor on immune function and susceptibility to upper respiratory infection; b) examines possible behavioral and neuroendocrine mediators of these relations; c) examines possible immune mediation of stressor influences on disease susceptibility; and d) investigates stable personal characteristics that might directly influence or moderate stressor-elicited immune modulation or stressor-elicited susceptibility to infection. In our study, healthy male cynomolgus monkeys who have spent prolonged periods (8 or 16 months) in stressful or nonstressful social situations are challenged with one of two influenza viruses. Prior to challenge, each animal is assessed for two temporally and situationally stable personal characteristics, social status and heart rate responsivity. Primary outcomes include immune response, infection (viral shedding as detected by in vitro culture techniques or by ELISA for viral antigen) and clinical disease (infection plus symptomatology). Behavioral responses to the social stressor are coded and sympathetic and pituitary- mediated hormonal response assessed. These data can provide important clues to the role of psychosocial factors in primary AIDS infections as well as help delineate conditions under which latent and subclinical AIDS infections progress to clinical disease.